Bacterial infection in wounds, especially burn-related wounds in children, is a major clinical problem in hospitals [D. Church et at (2006)]. Burn victims who are young children are particularly vulnerable to and at risk of infection due to immature immune systems, yet they are often a neglected patient group in the UK National Health Service (NHS) [Sir I. Kennedy (2010)]. In the UK, children under five years of age make up only 8% of the population but receive 53% of all serious scald burns with subsequent physiological and psychological effects [NBCR (2001)]. In general about 10% of all serious scald burns become infected, resulting in delayed healing, scarring, increased morbidity and mortality rates [UK Burn Injury Data (1986-2007)]. Burn wounds are different from other wounds, such as chronic wounds, in many aspects and therefore means of clinical diagnosis and treatment for wounds in general cannot be simply adopted for burn wounds [FDA (2006)]. Clinical symptoms of infection in burn wounds are very similar to the normal inflammatory response to a burn, and sepsis imposes difficulties in early detection of bacterial infection, thereby hindering effective treatment before the infection spreads uncontrollably [D. Church et al (2006)]. As a preventive measure to infection, paediatric burn victims are often treated with systematic antibiotics without concrete proof of a burn related ‘actual’ infection, thereby increasing healthcare antibiotic resistance. This has contributed to the evolution and increased resistance of pathogenic bacteria to the present day's antibiotics.
Current clinical treatment of burn wounds includes removal of debris, cleaning and application of a dressing, which effectively sterilises and seals the burn area [J. Wasiak et at (2009)]. This is followed by clinical observation and direct wound assessment for the possible initiation of infection as wound healing is in progress. Bacterial infection is still possible, though, if bacteria from the surrounding non-sterile skin enter the wound under the dressing. This is more likely to happen when direct wound assessment such as frequent removal and replacement of the dressing is required. Even if the burn wound is not infected, repeated changes of dressings extend the normal healing time, requiring a longer hospital stay and increasing the chance of scarring and trauma with additional concomitant costs. Hence, there is an urgent requirement for the ability to diagnose and identify burn wound infection, or absence thereof, without removal of expensive dressings. An alternative approach is the use of dressings impregnated with antimicrobial compounds such as silver ions for suppression of microbial growth. Despite the effectiveness of antimicrobials against bacteria, antimicrobial compounds such as silver may be partially cytotoxic to healthy cells and may also suppress tissue re-growth of wounds [V. K. M. Poon and A. Burd (2004)]. Importantly, continuous exposure of the wound to the antimicrobial agents is not a viable solution for preventive treatment of infection as this could increase the rate of evolution of bacteria resistance [A. T. A. Jenkins and A. E. Young (2010)].
Two main species of pathogenic bacteria commonly found in burn-related wound infections are S. aureus and P. aeruginosa [L. K. Branski et al. (2009)]. S. aureus is the gram-positive human pathogen persistently colonized on human skin flora. Most S. aureus strains are known to be pathogenic due to numerous secreted virulence factors including alpha, gamma and delta pore-forming toxins (PFTs), cholesterol binding toxins (CBTs) [R. J. C. Gilbert (2002)], and toxic shock toxins (TST) [M. M. Dinges et al. (2000) and S. Tangpraphaphorn (2004)]. TST is a major cause of toxic shock syndrome (TSS) Which functions by means of over-activation of the host immune system response. If not treated, TSS can cause death to the host within hours [A. E. Young and K. L. Thornton (2007), V. E. Jones (2006)]. The other principal agent, P. aeruginosa, is a gram-negative human opportunistic pathogen and is responsible for, amongst others, fatal infections in patients with cystic fibrosis and immuno-suppression [L. K. Branski et al. (2009)]. It is also found in human skin flora and is associated with various virulence factors for suspected lysis of healthy eukaryotic cells and tissue matrices upon infection. PFTs of S. aureus and lipid-degrading enzymes such as phospholipases of P. aeruginosa are proven to be able to lyse cell membranes or healthy cells in vivo and in vitro [J. G. Songer (1997), P. V. Liu (1974), M. M. Dinges et al (2000) and J. L. Arpigny and K. E. Jaeger (1999)]. Subject to the mode of action of particular lypolytic toxins of bacteria, pathogenic strains of S. aureus and P. aeruginosa were detected and discriminated from commensal E. coli bacteria by biomimetic lipid bilayer membrane on a gold surface using electrochemical impedance spectroscopy (EIS) and surface Plasmon resonance (SPR) [N. T. Thet and A. T. A. Jenkins (2010) and N. T. Thet et al (2011)]. A prototype wound dressing technology has been developed that can detect wound infection by pathogenic bacteria and alert clinicians automatically. It uses lipid vesicles containing fluorescent dyes attached to fabrics. [J. Zhou et al (2011)].
It would be particularly advantageous to be able to diagnose infection swiftly and simply, particularly if that diagnosis could identify the bacteria or type of bacteria responsible. Specifically, it would be advantageous to be able to identify the presence, or absence, of the bacteria most likely to cause infection in a burn wound, and to distinguish between these bacteria, if possible.